Effects of peroxisome proliferator-activated receptor γ agonist on serum adiponectin,urine microalbumin and renal pathology of obese mice

Objective To investigate the effects of peroxisome proliferator-activated receptor γ (PPARγ) agonist on serum adiponectin (ADP), urine microalbumin (mALB) and kidney pathology of obese mice, and discuss the significance of PPARγ agonists preventing obesity-related glomerulopathy (ORG). Methods Sixteen male ob/ob mice and 8 male C57BL/6 mice which were 8 weeks old were selected in this study. Ob/ob mice were dividing into 2 groups according to body mass: obesity group (M group) and pioglitazone intervention group (T group) which were fed with high lipid chow. C57BL/6 mice were control group (C group) which were fed with ordinary chow for 12 weeks. Body mass, blood glucose, serum ADP, urine mALB were assayed in each group and compared. The morphological changes of kidney were observe by HE staining, glomerular diameters were measured and compared. Zonula occludens-1 (ZO-1) and Wilms tumor 1 (WT1) were positioned by immunohistochemistry, the level of ZO-1 expression in podocyte and podocyte number which was signed with WT1 in each group were evaluated and compared. And then the correlations between serum ADP, urine mALB, body mass, blood glucose, kidney mass, glomerular diameter, the level of ZO-1 expression, podocyte number were analyzed. Results The serum ADP of obese mice decreased (P＜0.05), and the urine mALB increased (P＜0.05), when compared with that of control group, and there was a negative correlation between ADP and mALB (r＝-0.538, P＜0.01). Renal pathology showed glomerular hypertrophy, in part associated with focal segmental glomerulosclerosis (FSGS), the expression of ZO-1 in podocyte and podocyte number were lower than that of control group (P＜0.05). After the intervention with pioglitazone, the urine mALB of obese mice reduced (P＜0.01), and the serum ADP level of them was higher than that of obese mice without intervention (P＜0.01). There was no glomerular hypertrophy and glomerulosclerosis in kidney of obese mice, the expression of ZO-1 in podocyte and podocyte number were higher than that of obese mice without intervention (P＜0.05). Conclusions The kidneys of obese mice have clinical and pathological changes indicating that obesity can lead to kidney damage. Pioglitazone can make the low serum ADP level of obese mice ameliorated, and make the urine mALB of them reduced. Renal pathological change significantly is alleviated, the expression of ZO-1 in podocyte and podocyte number are increased, indicating pioglitazone can improve renal injury related to obesity.